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Chemokine signalling: pivoting around multiple phosphoinositide 3-kinases
Adam P Curnock1, Marisa K Logan, Stephen G Ward
1Department of Pharmacy and Pharmacology, Bath University, Claverton Down, Bath, Avon BA2 7AY, UK.
Immunology
|March 2, 2002
Summary
Chemokines guide cell movement by activating phosphoinositide 3-kinase (PI3K) signaling pathways. This review details how PI3K and its targets mediate chemokine-driven migration of inflammatory cells.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Chemokines are crucial for directing cell migration.
- Emerging evidence shows chemokines activate signaling pathways beyond chemotaxis, including cell growth and gene expression.
- The phosphoinositide 3-kinase (PI3K) pathway is a key focus in understanding chemokine-mediated cellular functions.
Purpose of the Study:
- To review the role of PI3K signaling in chemokine-mediated cell migration.
- To explore the involvement of specific PI3K isoforms and their downstream targets.
Main Methods:
- Literature review of biochemical, pharmacological, and genetic studies.
- Analysis of evidence linking CC and CXC chemokines to PI3K-dependent cell migration.
Main Results:
- Chemokine-induced chemotaxis of inflammatory cells (eosinophils, macrophages, neutrophils, T lymphocytes) is PI3K-dependent.
- Specific PI3K isoforms, including p85/p110 heterodimer, PI3Kgamma, and PI3KC2alpha, are implicated.
Conclusions:
- PI3K signaling is essential for chemokine-driven migration of inflammatory cells.
- Understanding individual PI3Ks and their effectors provides insight into inflammatory cell trafficking.